Can paracetamol (acetaminophen) overdose cause bilateral lower limb motor and sensory deficits?

Paracetamol Overdose and Bilateral Lower Limb Motor and Sensory Deficits

Paracetamol (acetaminophen) overdose does not typically cause bilateral lower limb motor and sensory deficits as part of its toxicity profile, as the primary target organ for paracetamol toxicity is the liver rather than the nervous system. 1

Primary Effects of Paracetamol Overdose

• Paracetamol overdose primarily causes dose-dependent hepatotoxicity, which can progress to acute liver failure in severe cases 2
• The main clinical manifestations of paracetamol toxicity include:
  • Hepatic injury (elevated liver enzymes, coagulopathy) 3
  • Gastrointestinal symptoms (nausea, vomiting, abdominal pain) 4
  • In severe cases, hepatic encephalopathy may develop, which presents with altered mental status rather than focal neurological deficits 5

Neurological Manifestations in Paracetamol Overdose

• Neurological symptoms in paracetamol overdose are typically related to hepatic encephalopathy secondary to liver failure, not direct neurotoxicity 5
• Hepatic encephalopathy presents with:
  • Altered mental status (confusion, drowsiness) 5
  • Asterixis (flapping tremor) 1
  • Global neurological dysfunction 1
• Importantly, hepatic encephalopathy does not cause focal neurological deficits such as isolated bilateral lower limb motor and sensory deficits 1, 5

Time Course of Paracetamol Toxicity

• Paracetamol toxicity follows a predictable pattern:
  • Phase 1 (0-24 hours): Nonspecific symptoms like nausea, vomiting 4
  • Phase 2 (24-72 hours): Right upper quadrant pain, rising liver enzymes 3
  • Phase 3 (72-96 hours): Peak liver injury, possible hepatic encephalopathy 5
  • Phase 4 (4-14 days): Recovery or progression to death 6
• At no point in this progression is bilateral lower limb motor and sensory deficit a recognized manifestation 1

Differential Diagnosis for Bilateral Lower Limb Deficits

If a patient presents with paracetamol overdose and bilateral lower limb motor and sensory deficits, clinicians should consider:

• Alternative toxins or co-ingestants that may have neurotoxic properties 1
• Spinal cord compression from positioning during prolonged unconsciousness 1
• Rhabdomyolysis-induced compartment syndrome from prolonged immobility 1
• Unrelated neurological conditions coinciding with the overdose 1

Conclusion

When evaluating a patient with bilateral lower limb motor and sensory deficits following paracetamol overdose, it is essential to recognize that these neurological findings are not directly attributable to paracetamol toxicity and warrant investigation for alternative causes 1.